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Exercise & Environment > Hormone use and abuse in sports > Flashcards

Hormone use and abuse in sports Flashcards

1
Q

WADA

A

world anti doping agency

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2
Q

prohibited substances

A
  • anabolic agents
  • peptide hormones, growth factor and related substances and memetic
  • beta-2 agonists
  • hormone and metabolic modulators
  • diuretics
  • masking agents
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3
Q

why are dieuretics used

A

short term weight loss

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4
Q

which sports is beta 2 agonist popular in

A

cycling

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5
Q

prohibited methods

A
  • manipulation of blood & components
  • chemical and physical
  • gene doping
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6
Q

substances and methods prohibited in competition

A
  • stimulants
  • narcotics
  • cannabinoids
  • glucocorticoids
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7
Q

substances prohibited in particular sports

A
  • alcohol in snooker
  • beta blockers in shooting
  • narcotics
  • cannabinoids
  • glucocorticoids
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8
Q

TUEs

A

therapeutic exemption certificates
e.g lots of cyclists seem to have been prescribed beta agonists and formally declared to have asthma, for bonafide reasons

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9
Q

what supplement is curet under questioning for it s administration and dosage

A

L-carnitine

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10
Q

L-carnitine

A
  • involved in mitochondrial FA translocation
  • during high intensity exercise, formation of acetylcarnitine is essential for maintenance of a viable pool of free co-enzyme A
  • this enables PDC & TCA flux to continue
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11
Q

what is the legal asthma drug, found to have been taken at 2 times the allowed level by chris froome

A

Beta 2 agonist

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12
Q

doping for strength and power training target

A

muscle mass

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13
Q

doping for endurance training target

A

aerobic metabolism

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14
Q

three key drugs for doping

A
  • testosterone
  • growth hormone
  • erythropoietin
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15
Q

what is focus of body building

A

aesthetics not function and strength

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16
Q

what axis is critical in muscle growth and developemet

A

GH - IGF1 axis

GH stimulates release of IGFI from the liver.
Muscle takes up IGF1, releases IGF1 and self produces IGF1

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17
Q

effect of IGF1 on muscle

A
  • causes proliferation and differentiation of satellite cells
  • stimulates MPS
  • inhibits MPB
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18
Q

what does direct infusion of IGF1 do to mice muscles

A
  • causes growth

- has insulin like properties

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19
Q

rhGH

A

recombinant human growth hormone

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20
Q

effects of rhGH

is it anabolic?

A
  • increases circulating IGF1
  • doesn’t increase MPS over and above resistance training

studies show its not anabolic ^
however shown to strengthen connective tissue structure and tendons hence prohibited

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21
Q

why is rhGH prohibited

A

shown to have little to no anabolic effects BUT
- doesn’t effect MPS
- shown to effect CPS
- found in tendons
= strengthens connective tissues structure and tendons which means less injury

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22
Q

what strengthens connective tissues structure and tendons which means less injury

A

rhGH

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23
Q

CPS

A

collagen protein synthesis

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24
Q

anabolic-androgenic steroid

A

testosterone derivatives

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25
Q

how to get best results from testosterone

A

couple with exercise. Exercise and testosterone give additive effects

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26
Q

hypertrophy

A

muscle fibre growth

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27
Q

hyperplasia

A

more muscle fibres

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28
Q

most common form of muscle growth in humans

A

hypertrophy - increased muscle fibre area

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29
Q

effects of testosterone

A
  • increased fibre area

- increased satellite cell number and myonuceli number in dose-response manner

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30
Q

what does testosterone act on

A
  • androgen receptors

- myonuclei satellite cells

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31
Q

what gives testosterone a potential longer term advantage

A

the increase in myonuclei satellite cells remain for many at least 2 years, becuase they have a very slow turn over. This means that upon training, greater hypertrophy can still be obtained once administration has stopped
= muscle memory

performed in rats, not humans, Begs question of how long ban should be

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32
Q

can steroids be used to help increase muscle mass of the elderly?

A

steroids wil give a 3% increase in muscle muscle and final performance

  • athletes are finally tuned machines, 3% is a big difference
  • elderly are not working at optimum and so improvement would be negligible. They would benefit more from excercise
  • there are also lots of side effects to steroid use
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33
Q

summary of IGF-1 use

A
  • local action is important
  • activates canonical pathway, but debatable as to whether it is essential for hypertrophy
  • GH increases circulation IGF-1 but does not increases MPS
  • GH does increase CPS
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34
Q

summary of testosterone use

A
  • hypertrophic at pharmacological doses
  • when knocked out it ameliorates normal hypertropgy
  • carting levels within physiological range seem to have no effect
  • not a linear dose-response relationship
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35
Q

male side effects of anabolic steroids

A
  • baldness
  • reduced sperm count
  • breast development
  • shrunken testicles
  • increased risk of prostate cancer
  • splayed teeth
  • overgrown forehead
  • severe acne
36
Q

female side effects of anabolic steroids

A
  • facial and body hair growth
  • loss of breasts
  • swelling of clitoris
  • deepened voice
  • increased sex drive
  • problems with periods
  • hair loss
  • sever acnes
37
Q

serious side effects of anabolic-androgenic steroids (AAS)

A
  • heart attack or stroke
  • kidney or liver tumour
  • hypertension
  • blood clots
  • fluid retention
  • high cholesterol
  • prostate cancer
38
Q

AAS

A

anabolic-androgenic steroids

39
Q

gene doping

A

misuse of gene therapy
- the non-therapeutic use of genes, genetic elements and or cells that have the capacity to enhance athletic performance (WADA ‘01)

40
Q

principle of gene therapy

A
  • delivery to a cell of a therapeutic gene that may correct an abnormal gene
  • directed primarily at a single gene disorder e.g muscular dystrophy, CF
  • bodies improve NATURALLY post gene doping making it difficult to detect
41
Q

why is gene doping hard to detect

A

because bodies improve/change naturally post GD

42
Q

2 basic types of gene transfer

A
  • germ line gene transfer / transgenesis

- somatic gene transfer

43
Q

germ line gene transfer

A
  • genetic material injected into nucleus of an early embryo before differentiation into somatic cells
  • ensures that the GM is present in all cells and future generations
  • not currently possible in humans = master breed
44
Q

somatic gene transfer

A
  • changing gene in an adult

- basis of gene therapy

45
Q

what functions are targeted by gene therapy

A
  • improving muscle mass strength
  • improving oxygen delivery
  • improving oxygen utilisation
46
Q

genes that improve muscle mass strength

A

IGF1

Myostatin

47
Q

genes that improves oxygen delivery

A

EPO

VEGF

48
Q

genes that increase oxygen utilisation

A

PGC-1a
PPAR delta
PEPCK

49
Q

gene therapy for enhanced muscle mass

A

transgene manipulator of IGF-1 expression causes over expression of IGF-1 in localised muscle = increased muscle mass
MICE

50
Q

Findings of IGF-IEa gene transfer in rats

A

when combined with strength training, adaptations are enhanced

  • increased muscle mass
  • increased isometric force
51
Q

problem of transferring rat studies of IGF-IEa to humans

A

would need exactly the same levels of gene expression in both biceps for symmetry. Otherwise performance would be affects by balance etc.
Difficult to scale up

52
Q

what is the myostatin gene

A

GDF-8 is a negative regulator of muscle mass

53
Q

GDF-8

A

myostatin gene. negative regulator of muscle mass

54
Q

Belgian Blue Cattle

A

double muscle phenotype caused by lack of GDF-8 gene (myostatin)
shows association not prove causality

55
Q

what happens to GDF-8 knockout mice

A

hypertrophy

no brakes on muscle growth, GDF8 is an inhibitor of MPS

56
Q

effects of lacking in myostatin

A

results in excessive muscle growth BUT impaired force generation.
this is not a concern for body builders where aesthetics > performance

57
Q

what is blood doping used for

A

to increase VO2max

  • blood infused during VO2 max
  • done wrong, can causes death
58
Q

safer version of blood doping

A

EPO

59
Q

what is EPO

A

erythropoietin - medical therapy for kidney failure

60
Q

how does EPO work

A
  • glycoprotein produced by kidney in response to low oxygen
  • stimulates bone marrow to make more RBC
  • # synthetic EPO has same effect
  • increase in RBC for oxygen transport
  • increase VO2max for endurance
    BUT
    risk of increased viscosity of the blood = heart attack and stroke
61
Q

risk of EPO

A

increased viscosity of blood = hypotension = heart attack and stroke

62
Q

microdoping

A

small changes which are safer and harder to detect

63
Q

EPO mouse and monkey gene transfer studies

A
  • adenovirus was used to deliver EPO gene to mouse and monkeys
  • mouse hematocrits increase from 49-81%
  • monkeys hematocrits increased from 40-70%
    BUT blood thinning was required to keep animals alive becuase the EPO production had no switch off
  • body is an integrated system. If you change one thing, you will cause off targets effects of another which are usually dangerous
64
Q

why does doping have so many side effects

A

body is an integrated system. Change one thing and you will often get off-target effects of another part of the system which usually cause adverse effects

65
Q

VEGF

A

vascular endothelial growth factor

66
Q

application of VEGF

A
  • improves micro circulation
  • extensively tested in clinical trials for ischaemic efficacy in cardiac & skeletal muscle disease
  • limited success bc of complex regulation of angiogenesis
67
Q

microcirucaltion

A

microcirculation is the circulation of the blood in the smallest blood vessels, the microvessels of the microvasculature present within organ tissues

68
Q

ischaemic

A

inadequate blood supply to organ or part of body, particularly the heart muscle

69
Q

genes that increase oxygen utilisation

A

PGC-1alpha
PPAR delta
PEPCK

70
Q

PGC-1alpha

A
  • coactivator regualtion gene involved in energy metabolism
  • links external stimuli and regulation of mitochondrial biogenesis
  • master regulator of mitochondrial biogenesis
71
Q

PPAR delta

A

nuclear receptor proteins that function as transcription factors

72
Q

PEPCK

A

phosphoenolypyruvate carboxykinase

- rate limiting enzyme of gluconeogenesis

73
Q

rate limiting enzymes of gluconeogenesis

A

PEPCK

74
Q

effect of over expression of PCG-1alpha in transgenic mice

A
  • increased mitochondrial biogenesis bc master regulator
  • muscle appear redder due to myoglobin
  • cytochrome C is marker for increased mitochondrial content
  • motor protons such as slow troponin and slow myosin are unregulated which is unexpected
75
Q

unexpected results of over expression of PCG-1alpha in transgenic mice

A

Motor proteins such as slow troponin and slow myosin are unregulated

76
Q

what is the marker for mitochondrial content

A

cytochrome C

77
Q

effect of PPAR delta in mice

A
  • darker muscle fibres
  • more oxidative activity
  • more mitochondria
  • faster running time
78
Q

Paper on over expression of PEPCK

A 
was not a hypothesis driven paper. showed off-target effects of manipulation 
PEPCK mouse showed:
- greater distance ran
- RER below 1, so mostly burning fat
- more mitochondria
suggests that PEPCK gives endurance
79
Q

does over expression of PEPCK give endurance? base on mouse paper findings

A
  • PEPCK mouse showed changes for improved enduracne
    BUT, was this the result of PEPCK or greater training?
    the PEPCK ran further & longer, so unsure if the improvements are from the increased training or PEPCK.
    Did PEPCK cause the change in behaviour so they exercised more?
80
Q

Mouse to man for gene therapy

A
  • most gene therapy shows impressive results in animal models of human disease
  • but mice are small and tough creatures
    • most used high vector doses, how will these affect man?
  • -there was limited spread of any vector system used intramuscularly
    • much have small muscles which I’ve impressive results, how will this scale up to human muscle which are very large in comparisons
81
Q

risk of gene doing

A

uncontrolled expression!

  • EPO causes increased heamtocrit leading to stroke and heart failure
  • GH &IGF1 have risk of oncogenesis
  • insertional mutagenesis
  • myostatin reduces specific force
82
Q

Case studies of naturally occurring genetic advantage

A

Finnish cross country skier accused of blood doping in 1964

  • 15% more RBC than normal
  • EPO receptor mutation in family which removed the switch off EPO function

Myostatin mutation in young boy

  • born with v muscly phenotype
  • similar to belgian blues cow

should they be able to compete?

83
Q

what determines type of doping

A

physiological determinants of performance

84
Q

what is the overall goal of AAS use

A

increase muscle size, for aesthetics or strength and power

85
Q

what is the overall goal of EPO use

A

increase oxygen carrying capacity of blood and delivery, for improved endurance

86
Q

why is it difficult to test drugs taken by athletes

A

they take them at doses that are not ethically compatible with mainstream scientific research. Dose-Response effectiveness if subject to speculation

87
Q

Is gene doping a concern

A

been viewed as the new frontier of doping but no evidence of practising in sport, despite results in rodents.
There is a lot of problems with legitimacy and ethics of gene therapy

Exercise & Environment (14 decks)

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